Related Experiment Videos
Epidermal growth factor: a potent vasoconstrictor in experimental hypertension
1Department of Pharmacology and Toxicology, Michigan State University, East Lansing, Michigan 48824-1317, USA.
The American Journal of Physiology
|March 10, 1999
Summary
Hypertension augments epidermal growth factor (EGF) signaling in rat aorta, causing vasoconstriction. This suggests growth factors act as vasoconstrictors in hypertension, impacting vascular smooth muscle cell growth.
Area of Science:
- Cardiovascular Physiology
- Molecular Biology
- Hypertension Research
Background:
- Hypertension is linked to vascular smooth muscle cell growth.
- Growth factor signaling pathways may be augmented in hypertensive states.
- Epidermal growth factor (EGF) is a key signaling molecule.
Purpose of the Study:
- To test if growth factor signaling is augmented in hypertension.
- To investigate the role of EGF in hypertensive rat aorta.
- To determine if EGF acts as a vasoconstrictor in hypertension.
Main Methods:
- Dissection of thoracic aorta from DOCA-salt and 1K, 1C hypertensive rats and sham normotensive rats.
- Isolated tissue bath experiments to measure aortic contraction in response to EGF.
- Pharmacological inhibition of EGF receptor, MAPK pathway, calcium channels, and cyclooxygenase.
Main Results:
- EGF induced significant contraction in aorta from hypertensive rats, but not normotensive rats.
- EGF-induced contraction was observed by day 14 of DOCA-salt therapy, coinciding with elevated blood pressure.
- Inhibitors of EGF receptor tyrosine kinase, MEK, and L-type calcium channels abolished EGF-induced contraction.
Conclusions:
- EGF signaling is significantly augmented in hypertension, leading to vasoconstriction.
- Growth factors like EGF should be considered vasoconstrictors in hypertension.
- These findings highlight a critical difference in EGF signaling between normotensive and hypertensive states.